video feature depicting protein synthesis ..
Oregon State University, Corvallis, OR
Research Assistant, Dr. J.D. White | 1984 – 1987
Pharmaceutical synthesis; structure determination of protein and natural products; molecular modeling; drug delivery, particularly prodrug synthesis.
Protein synthesis: an epic on the cellular level
Instruction 1: You will be simulating the process of protein synthesis from DNA that occurs in every cell and the effects of mutations on the proteins that are produced.
This model allows you to explore the effects of deletion, substitution, and insertion mutations on a single strand of DNA and the subsequent outcomes in related protein synthesis in cells. The model represents effects from mutations that include 1) the number of genes that are encoded in the DNA, 2) the mRNA molecules that are transcribed, and 3) the tRNA molecules that are used to transcribe the mRNA into an amino acid chain, as wells as 4) the subsequent protein that is synthesized.
Protein Synthesis: An Epic on the Cellular Level (1971)
In order for DNA to produce proteins for each gene, the following four steps must be followed by the user, after GO/STOP is pressed to start running the model.
The Paul Berg Papers Title: Protein Synthesis: ..
El-Rady views the remake as a tribute to the 37-year-old original, but hopes that “Lost in Translation” will offer a modern, humorous take on protein synthesis for instructors and students.
Molecular Genetics I Video Lecture, Stanford
The tyrosine analog -propargyloxyphenylalanine (pPa), like tyrosine, has limited water solubility. It has been postulated that this limited solubility has contributed to reduced cellular uptake of pPa and thus reduced incorporation of pPa into proteins. Using a cell-free protein synthesis system (CFPS) to circumvent cellular uptake, pPa has been incorporated site-specifically into proteins with high specificity at yields up to 27 times greater than the highest previously reported yield. The alkyne group present on proteins incorporated with pPa provides a reactive residue for site-specific bioconjugation with the copper(I)-catalyzed azide−alkyne [3 + 2] cycloaddition (CuAAC). Previously, incorporation of another CuAAC-compatible unnatural amino acid -azido--phenylalanine (pAz) was demonstrated with CFPS. However, incorporation of pPa may be preferred over pAz due to the instability of the pAz’s aryl-azido moiety upon UV or near-UV light exposure. Also, the ability to incorporate site-specifically both reactants of the CuAAC (the alkyne group of pPa and the azido group of pAz) into proteins enables direct site-specific conjugation of heterologous proteins. We have demonstrated (for the first time to our knowledge) a one-step, linker-less, site-specific, direct protein-to-protein conjugation using CuAAC and unnatural amino acids.
Molecular Genetics I Video Lecture, Stanford Course, ..
Increased neuronal plasticity and neuronal cell loss has been implicated in the development of epilepsy following injury. Parvalbumin fast spiking inhibitory interneurons have a robust extracellular matrix coating their cell bodies and the proximal dendrites called the perineuronal net (PNN). The role of the PNN is not clear but it has been implicated in closing of the critical period, altering seizure thresholds and providing neuronal protection from oxidative stress. The PNN is susceptible to degradation following a prolonged seizure and there is an increase in proteolytic-fragments of the PNN enriched proteoglycan aggrecan (Dzwonek et al., 2004). Here we demonstrate an increase in matrix metalloproteinase (MMP) activity in the hippocampus following status epilepticus (SE). We further assessed MMP3 and 13, two of 24 identified MMPs, both MMP3 and 13 mRNA increase in the hippocampus after SE and MMP13 activity increases by functional assay as well as it co-localizes with PNN in rat brain. In contrast, two of the brain expressed ADAMTS (A Disintegrin And Metalloproteinase with ThromboSpondin motifs) also implicated in aggrecan degradation, did not consistently increase following SE though ADAMTS4 is highly expressed in glia and ADAMTS5 in neuronal cell bodies and their processes. The increase in MMP activity following SE suggests that in the future studies, MMP inhibitors are candidates for blocking PNN degradation and assessing the role of the PNN loss in epileptogenesis and cellular function.